Cirrhosis Hepatis Lapkas DR Toton
Cirrhosis Hepatis Lapkas DR Toton
1 2 3 4
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Kepala normochepal
Rambut : tidak rontok
Alis : tidak rontok
Mata : sklera ikterik,konjungtiva anemis
Hidung : tidak ada sekret keluar
Bibir : kering
Mulut : lidah tidak kotor, gusi tidak bengkak
Telinga : tidak ada serumen yang keluar
Leher : Pembesaran KGB (-), pembesaran tiroid (-/-),
JVP 5+3 cmH2O
Kesan : kardiomegali
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i: tampak cembung
a: BU 9x /min
p: Perut tampak membesar pemeriksaan shifting
dullness didapatkan perubahan suara timpani ke redup
begitupun sebaliknya ketika posisi dirubah/di miringkan.
p: tidak Teraba hati karena perut os membuncit
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* Acites dan hipoalbumin ec sirosis hepatis
* Dyspneu ec DC FC II stage C
* Anemia mikrositik hipokrom ec penyakit kronis
Causes of ascites
CMDT 2015
The clinical features of cirrhosis result from hepatocyte
dysfunction, portosystemic shunting, and portal hypertension.
Patients may have no symptoms for long periods. The
onset of symptoms may be insidious or, less often, abrupt.
Fatigue, disturbed sleep, muscle cramps, and weight loss
are common. In advanced cirrhosis, anorexia is usually
present and may be extreme, with associated nausea and
occasional vomiting, as well as reduced muscle strength
and exercise capacity. Abdominal pain may be present and
is related either to hepatic enlargement and stretching of
Glisson capsule or to the presence of ascites.
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* Ascites, pleural effusions, peripheral edema, and
ecchymoses are late findings. Encephalopathy
characterized by day–night reversal, asterixis,
tremor, dysarthria, delirium, drowsiness, and
ultimately coma also occurs late except when
precipitated by an acute hepatocellular insult or an
episode of gastrointestinal bleeding or infection.
Fever may be a presenting symptom in up to 35% of
patients.
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* Laboratory abnormalities are either absent or minimal in
early or compensated cirrhosis. Anemia, a frequent
finding,is often macrocytic; causes include suppression
of erythropoiesis by alcohol as well as folate deficiency,
hemolysis,hypersplenism, and occult or overt blood loss
from the gastrointestinal tract. The white blood cell
count may be low, reflecting hypersplenism, or high,
suggesting infection.Thrombocytopenia, the most
common cytopenia in cirrhotic patients, is secondary to
alcoholic marrow suppression, sepsis, folate deficiency,
or splenic sequestration. Prolongation of the prothrombin
time may result from reduced levels of clotting factors
(except factor VIII). However, bleeding risk correlates
poorly with the prothrombin time because of
concomitant abnormalities of fibrinolysis, and among
hospitalized patients under age 45, cirrhosis is associated
with an increased risk of venous thromboembolism.
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* Inf.asering 20 gtt/hari
* Inf albumin 20% 100 cc
* Spironolacton 1x100 mg
* Furosemid 1x20 mg
* Vit.K 3x1
* Curcuma 3x1
* Pct 3x500
1. The most important principle of treatment is
abstinence from alcohol
2. The diet should be palatable, with adequate
calories(25-35kcal/kgbb) and protein (1-1.2
g/kg/d)if malnutrition (1.5 g/kg/d)
3. Spironolactone, generally in combination
with furosemide, should be used in patiens
who do not respond to salt restriction.
furosemid 80 mg iv, spironolactone 100 mg daily
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CMDT 2015
*Assesment
2. Decomp Cordis kanan kiri Fc.II Stage C
Kriteria Frammingham
Kelas I
Aktivitas fisik tidak terganggu, aktivitas yang umum dilakukan tidak
menyebabkan kelelahan, palpitasi, atau sesak nafas.
Kelas II
Aktivitas fisik sedikit terbatasi. Saat istirahat tidak ada keluhan.
Tapi aktivitas fisik yang umum dilakukan mengakibatkan kelelahan,
palpitasi atau sesak nafas.
Kelas III
Aktivitas fisik sangat terbatasi. Saat istirahat tidak ada keluhan.
Tapi aktivitas ringan menimbulkan rasa lelah, palpitasi, atau sesak
nafas.
Kelas IV
Tidak dapat beraktivitas tanpa menimbulkan keluhan. Saat istirahat
bergejala. Jika melakukan aktivitas fisik, keluhan bertambah berat.
27
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* Bysoprolol 1x5 mg
* Digoxin 1x 0.25 mg
* Furosemid 1x20 mg
29
Progressive worsening of hepatocellular function in
cirrhosis can result in a fall in the concentration of
albumin and other serum proteins synthesized by
the liver. As the concentration of these plasma
protein decreases, the plasma oncotic pressure is
lowered, thereby tilting the balance of
hemodynamic forces toward the development
peripheral edema and acites
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MCV NORMAL
MCH NORMAL MCHC NORMAL
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CMDT 2011
* Anemia normositik normokrom
Etiologi :
1. Hemolitik anemia
2. Pasca perdarahan akut
3. Anemia aplastik
4. Chronic renal failure
5. Anemia pada penyakit hati kronik
CMDT 2015
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HEMATOLOGY IN CLINICAL
PRACTICE fifth edition
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* Inf.asering 20 gtt/hari
* Inf albumin 20% 100 cc
* Spironolacton 1x100 mg
* Furosemid 1x20 mg
* Vit.K 3x1
* Bysoprolol 1x5 mg
* Digoxin 1x 0.25 mg
* Curcuma 3x1
* Pct 3x500
Tanggal 1/12/15
Subject Sesak semalaman,bengkak pada kaki dan perut,nyeri perut
Object . Td 140/90, nadi 102x/mnt ireguler, fp 20x/mnt,suhu 37C CA
+/+, si+/+JVP 5+3cmH2O, Thoraks Ka=ki, retraksi IC -, VBS +/+,
Rhonki basah halus +/+, wheezing -/-
Hepar dan lien tidak teraba
Nyeri tekan abd (-)
Edema -/-
+/+